Host response to cytomegalovirus infection as a determinant of susceptibility to coronary artery disease - Sex-based differences in inflammation and type of immune response
Jh. Zhu et al., Host response to cytomegalovirus infection as a determinant of susceptibility to coronary artery disease - Sex-based differences in inflammation and type of immune response, CIRCULATION, 102(20), 2000, pp. 2491-2496
Citations number
27
Categorie Soggetti
Cardiovascular & Respiratory Systems","Cardiovascular & Hematology Research
Background-Positive and negative associations between cytomegalovirus (CMV)
infection and coronary artery disease (CAD) have been reported. We postula
ted that the susceptibility to CMV-induced CAD might relate to patterns of
inflammatory and immune responses to CMV infection and that sex might have
an effect on these responses.
Methods and Results-In 151 men and 87 women being evaluated for CAD, blood
samples were tested for humoral (Ab+) and cellular (Tc+) responses to CMV a
nd for C-reactive protein (CRP). In men, an elevated CRP level was a signif
icant determinant of CAD even after adjustment for CAD risk factors (OR, 3.
1; 95% CI, 1.21 to 7.97). CMV seropositivity was associated with elevated C
RP levels on multivariate analysis (P=0.006). In contrast, in women, CMV se
ropositivity was independently predictive of CAD (OR, 41.8; 95% CI, 4.12 to
423.74). CRP level in women with CAD was >25% higher than those without CA
D, but the difference did not reach statistical significance. Importantly,
compared with CMV Ab-/Tc- women, CAD prevalence was higher in Ab+/Tc- and A
b+/Tc+ (13% versus 68% and 64%, both P<0.005) but not in Ab-/Tc+ women (25%
). There were no differences in age, smoking, diabetes, hypertension, and h
ypercholesterolemia among women with different types of immune responses to
CMV infection.
Conclusions-The mechanisms by which CMV predisposes to CAD in men and women
may be different. In men, CMV appears to contribute to CAD risk, insofar a
s it predisposes to inflammation. In women, other mechanisms, possibly rela
ted to the type of immune response generated by the host, appear to be resp
onsible for the proatherogenic effects of CMV.